Pulmonary Hypertension and COVID-19

2021 ◽  
Author(s):  
Laura Castiglione ◽  
Michal Droppa
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Arterial Pressure ◽  
Cardiovascular Complications ◽  
Ventricular Failure ◽  
Pulmonary Hemodynamics ◽  
Increased Risk ◽  
Systolic Pulmonary Arterial Pressure ◽  
Pulmonary Arterial ◽  
Randomized Control ◽  
The City

AbstractCoronavirus disease 2019 (COVID-19) is a primary respiratory infectious disease, which can result in pulmonary and cardiovascular complications. From its first appearance in the city of Wuhan (China), the infection spread worldwide, leading to its declaration as a pandemic on March 11, 2020. Clinical research on SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) suggests that the virus may determine changes in the pulmonary hemodynamics through mechanisms of endothelial dysfunction, vascular leak, thrombotic microangiopathy, and venous thromboembolism that are similar to those leading to pulmonary hypertension (PH). Current available studies report echocardiographic signs of PH in approximately 12 to 13% of hospitalized patients with COVID-19. Those with chronic pulmonary obstructive disease, congestive heart failure, pulmonary embolism, and prior PH are at increased risk to develop or worsen PH. Evidence of PH seems to be associated with increased disease severity and poor outcome. Because of the importance of the pulmonary hemodynamics in the pathophysiology of COVID-19, there is growing interest in exploring the potential therapeutical benefits of inhaled vasodilators in patients with COVID-19. Treatment with inhaled nitric oxide and prostacyclin has shown encouraging results through improvement of systemic oxygenation, reduction of systolic pulmonary arterial pressure, and prevention of right ventricular failure; however, data from randomized control trials are still required.

scholarly journals Impact of Elevated Parathormone Levels on the Severity of Pulmonary Hypertension in Patients with End Stage Renal Disease Undergoing Hemodialysis

2020 ◽  
Vol 71 (1) ◽  
pp. 298-301
Author(s):  
Cristina Tudoran ◽  
Mariana Tudoran ◽  
Ancuta Mates ◽  
Gheorghe Nicusor Pop ◽  
Ahmed Abu-Awwad
Keyword(s):  
Pulmonary Hypertension ◽  
Renal Disease ◽  
End Stage Renal Disease ◽  
Pulmonary Arterial Pressure ◽  
Cardiovascular Complications ◽  
Systolic Pulmonary Artery Pressure ◽  
Systolic Pulmonary Arterial Pressure ◽  
Pulmonary Arterial ◽  
Stage Renal Disease ◽  
End Stage

One of the most severe cardiovascular complications encountered in patients with end stage renal disease (ESRD) undergoing hemodialysis (HD) is pulmonary hypertension (PH). Secondary hyperparathyroidism (SHPTH) is supposed to be one of the contributing mechanisms responsible for the occurrence of PH in these patients.The aim of our study is to determine if the elevated values of intact parathormone (iPTH) are correlated with increased pulmonary vascular resistance (PVR) in patients ESRD undergoing HD.Our study was conducted on 51 patients with ESRD undergoing HD. We assessed in all patients the levels of iPTH, as well as the systolic pulmonary arterial pressure (PAPs) and PVR by means of echocardiography. According to the levels of PAPs, patients were classified into two subgroups: 27 with 24 without PH.We documented a moderate correlation between iPTH and systolic pulmonary artery pressure (PAPs), respectively PVR in patients with PH. In patients without PH there were no significant correlations between iPAH and PVR, respectively PAPs.

MO746CARDIAC REMODELING AND PULMONARY HYPERTENSION IN HEMODIALYSIS PATIENTS

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Ekaterina Borodulina ◽  
Alexander M Shutov
Keyword(s):  
Pulmonary Hypertension ◽  
Left Ventricular Hypertrophy ◽  
Arterial Pressure ◽  
Ventricular Hypertrophy ◽  
Pulmonary Arterial Pressure ◽  
Hemodialysis Patients ◽  
Left Ventricular ◽  
Hemodialysis Treatment ◽  
Systolic Pulmonary Arterial Pressure ◽  
Pulmonary Arterial

Abstract Background and Aims An important predictor of cardiovascular mortality and morbidity in hemodialysis patients is left ventricular hypertrophy. Also, pulmonary hypertension is a risk factor for mortality and cardiovascular events in hemodialysis patients. The aim of this study was to investigate cardiac remodeling and the dynamics of pulmonary arterial pressure during a year-long hemodialysis treatment and to evaluate relationship between pulmonary arterial pressure and blood flow in arteriovenous fistula. Method Hemodialysis patients (n=88; 42 males, 46 females, mean age was 51.7±13.0 years) were studied. Echocardiography and Doppler echocardiography were performed in the beginning of hemodialysis treatment and after a year. Echocardiographic evaluation was carried out on the day after dialysis. Left ventricular mass index (LVMI) was calculated. Left ventricular ejection fraction (LVEF) was measured by the echocardiographic Simpson method. Arteriovenous fistula flow was determined by Doppler echocardiography. Pulmonary hypertension was diagnosed according to criteria of Guidelines for the diagnosis and treatment of pulmonary hypertension of the European Society of Cardiology. Results Pulmonary hypertension was diagnosed in 47 (53.4%) patients. Left ventricular hypertrophy was revealed in 71 (80.7%) patients. Only 2 (2.3%) patients had LVEF<50%. At the beginning of hemodialysis correlation was detected between systolic pulmonary arterial pressure and LVMI (r=0.52; P<0.001). Systolic pulmonary arterial pressure negatively correlated with left ventricular ejection fraction (r=-0.20; P=0.04). After a year of hemodialysis treatment LVMI decreased from 140.49±42.95 to 123.25±39.27 g/m2 (р=0.006) mainly due to a decrease in left ventricular end-diastolic dimension (from 50.23±6.48 to 45.13±5.24 mm, p=0.04) and systolic pulmonary arterial pressure decreased from 44.83±14.53 to 39.14±10.29 mmHg (р=0.002). Correlation wasn’t found between systolic pulmonary arterial pressure and arteriovenous fistula flow (r=0.17; p=0.4). Conclusion Pulmonary hypertension was diagnosed in half of patients at the beginning of hemodialysis treatment. Pulmonary hypertension in hemodialysis patients was associated with left ventricular hypertrophy, systolic left ventricular dysfunction. After a year-long hemodialysis treatment, a regress in left ventricular hypertrophy and a partial decrease in pulmonary arterial pressure were observed. There wasn’t correlation between arteriovenous fistula flow and systolic pulmonary arterial pressure.

scholarly journals Echocardiography in Confirmed and Highly Suspected Symptomatic COVID-19 Patients and Its Impact on Treatment Change

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Nadia Benyounes ◽  
Clélie Van Der Vynckt ◽  
Séverine Tibi ◽  
Alexandra Iglesias ◽  
Laurence Salomon ◽  
...  
Keyword(s):  
Myocardial Injury ◽  
Pulmonary Arterial Pressure ◽  
Cardiovascular Complications ◽  
Treatment Change ◽  
Systolic Pulmonary Arterial Pressure ◽  
Treatment Changes ◽  
Impact On Treatment ◽  
Pulmonary Arterial ◽  
Multiple Levels ◽  
D Dimer

Background. COVID-19 interacts at multiple levels with the cardiovascular system. The prognosis of COVID-19 infection is known to be worse for patients with underlying cardiovascular diseases. Furthermore, the virus is responsible for many cardiovascular complications. Myocardial injury may affect up to 20% of the critically ill patients. However, echocardiography’s impact on the management of patients affected by COVID-19 remains unknown. Objectives. To explore echocardiography’s impact on the management of COVID-19 patients. Methods. This study was conducted from March 24th to April 14th, 2020, in a single center at Adolphe de Rothschild Foundation Hospital, Paris, France. All consecutive inpatients with laboratory and/or CT COVID-19 diagnosis were included in this study. Patients’ characteristics (clinical, biological, and imaging) and treatment change induced by echocardiography were collected and analyzed. Patients with and without treatment change induced by echocardiography were compared. Results. A total of 56 echocardiographies in 42 patients with highly suspected or confirmed COVID-19 were included in the final analyses. The median age was 66 (IQR 60.5–74). Echocardiography induced a treatment change in 9 cases (16%). The analyzed clinical data were not associated with any treatment change induced by echocardiography. D-dimer and Troponin levels were the only biological predictors of the induced treatment change. On echocardiography, higher systolic pulmonary arterial pressure and documented cardiac thrombi were associated with treatment changes in these patients. Conclusions. Echocardiography may be useful for the management of selected COVID-19 patients, especially those with elevated D-Dimer and Troponin levels, in up to 16% of patients.

scholarly journals P954 Paps / Actpo ratio indicator of pulmonary arterial ventricle coupling in normal subjects and in pulmonary hypertension

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
W Serra ◽  
L M Marangoni ◽  
M G Goldoni ◽  
A C Chetta
Keyword(s):  
Pulmonary Hypertension ◽  
Statistical Analysis ◽  
Right Ventricular ◽  
Interobserver Variability ◽  
Normal Subjects ◽  
Right Ventricular Failure ◽  
Ventricular Failure ◽  
Indirect Measure ◽  
Increased Risk ◽  
Pulmonary Arterial

Abstract In Pulmonary Hypertension (PH), the development of dilatation and right ventricular failure (RV) are signs of accelerated progression of the disease resulting in an increased risk of cardiac death, and right ventricular failure. Even the non-invasive assessment of the systolic blood pressure pulmonary artery (PAPs) by well-established doppler echocardiography, this does not give us a measure of ventriculo-pulmonary interaction. Some studies have shown the potential use of echocardiography to indirectly evaluate the PVR and the pulmonary outflow acceleration time (ACTPO), it should be a good correlated indirect measure. To have a measure of the ventriculo-pulmonary interaction, we used a parameter that contained information related to pulmonary pressure and a parameter that was an indicator of pulmonary vascular resistance. We have therefore called it PAPS / ACTPO ratio [strength / surface unit] / [time]. We wanted to study this parameter in apparently healthy subjects to code the normal range. From January 2017 to December 2017, we have studied 60 normal patients subjecting them to a complete two-dimensional echocardiographic / Doppler evaluation of the right function and hemodynamics. Echocardiographic imaging was performed using a Philips IE33 and a 3.5 MHz transducer (Philips Medical Systems, Andover, MA). We planned to evaluate this parameter in patients with Pulmonary Hypertension associated with systemic sclerosis. Statistical analysis. To test the diagnostic power of variables, ROC curves were extrapolated. AUC and cut-off point (max sensitivity + specificity) were also calculated. Pair of variables were correlated by using Pearson’s test. Significance was always set at 0.05. IBM SPSS 25.0 (IBM, Amork, NY) was always used for all the statistical tests. PAPs/ACTpo ratio was measured by two echocardiographers blinded to the clinical data in order to assess interobserver variability Results In normal subjects we found a mean PAPS / ACTPO ratio of 0.26, indicator of an optimal pulmonary arterial ventricle coupling. The first data derived from the only 19 patient analysis shows that those presenting pre-capillary pulmonary hypertension to cardiac catheterization have a PAPS/ACTPO ratio of 0.40 ± 0.05 . Interobserver variability was lower than 5% Conclusion PAPS / ACTPO ratio may be an indicator of pulmonary arterial ventricle coupling. Table 1 PAPs/Act PAPs NYHA 24m Tapse (mm) Act (msc) PVR WUmm/Hg.min.L CAT dx PAPs PAPs/Act R value ,877 ,491 -,076 -,901 ,820 ,795 Sig ,000 ,033 ,757 ,000 ,000 ,000 19 19 19 19 19 19 18 Statistical analysis

scholarly journals 0718 Hypoxemia and Pulmonary Hypertension in Patients with Concomitant Restrictive Ventilatory Defect and Sleep Apnea: The Overlap Syndrome

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A273-A273
Author(s):  
J Xie ◽  
Z Fan ◽  
J Wang ◽  
F Li
Keyword(s):  
Pulmonary Hypertension ◽  
Sleep Apnea ◽  
Oxygen Saturation ◽  
Vital Capacity ◽  
Pulmonary Arterial Pressure ◽  
Forced Expiratory Volume ◽  
Overlap Syndrome ◽  
Apnea Hypopnea Index ◽  
Systolic Pulmonary Arterial Pressure ◽  
Pulmonary Arterial

Abstract Introduction Patients with severe restrictive ventilatory defect (RVD) have hypoxemia and a high risk of pulmonary hypertension (PHTN). Sleep apnea (SA) aggravates the severity of nocturnal desaturation significantly. The aim of this study was to investigate the severity of hypoxemia and prevalence of PHTN in patient with the overlap syndrome (OS) of RVD and SA. Methods Patients referred for both sleep test and spirometry for suspected SA and RVD or obstructive ventilatory defect (OVD) were recruited prospectively from January-December, 2018. SA was determined by an apnea-hypopnea index ≥5/h; mean nocturnal oxygen saturation (meanSaO2), minimum oxygen saturation (minSaO2), saturation lower than 90% (T90) were calculated automatically. RVD was diagnosed in the presence of forced expiratory volume in the first second/forced vital capacity (FVC) >0.7 and FVC<80% predicted value. PHTN was defined by systolic pulmonary arterial pressure (SPAP) ≥ 50mmHg, documented by noninvasive transthoracic echocardiography. Patients with PHTN secondary to extrapulmonary factors were excluded. Results Of 65 patients who completed the investigation, 16 (24.6%) subjects were diagnosed with isolated SA (without RVD or OVD), and 28 (43.1%) subjects were verified to have RVD, in which 22 (78.6%) were diagnosed with OS and 6 (21.4%) presented as isolated RVD. Patients with OS vs. those with isolated RVD had lower minSaO2 (78.3% vs. 88.7%, p=0.003) and meanSaO2 (91.5% vs. 95.8%, p=0.007) but higher T90 (37.2% vs. 0.3%, p=0.009). Patients with OS vs. those with isolated RVD or with isolated SA had higher SPAP (62.6 mmHg vs. 45.3 mmHg or 35.9 mmHg, p=0.334 or p=0.016 respectively). Higher proportion of patients with OS were diagnosed with PHTN than those with isolated RVD or isolated SA (8 [36.4%] vs. 1 [16%] or 1 [6.25%], p=0.360 or p=0.031, respectively). T90 was the only polysomnographic data associated with the prevalence of PHTN after adjusting for age and sex (OR 4.90, 95% CI 1.23-25.56, p=0.023). Conclusion Patients with the OS of RVD and SA had high odds of PHTN, which is probably associated with severe hypoxemia. Further investigation is needed to discern whether therapeutic strategies toward OS might eliminate PHTN in this cohort. Support  

Effects of inhaled nitric oxide at rest and during exercise in idiopathic pulmonary fibrosis

2011 ◽  
Vol 110 (3) ◽  
pp. 638-645 ◽  
Author(s):  
Isabel Blanco ◽  
Jesús Ribas ◽  
Antoni Xaubet ◽  
Federico P. Gómez ◽  
Josep Roca ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Hypertension ◽  
Gas Exchange ◽  
Pulmonary Arterial Pressure ◽  
Submaximal Exercise ◽  
Pulmonary Hemodynamics ◽  
Mean Pulmonary Arterial Pressure ◽  
Prostaglandin F ◽  
Pulmonary Arterial ◽  
Inhaled No

Patients with idiopathic pulmonary fibrosis (IPF) usually develop hypoxemia and pulmonary hypertension when exercising. To what extent endothelium-derived vasodilating agents modify these changes is unknown. The study was aimed to investigate in patients with IPF whether exercise induces changes in plasma levels of endothelium-derived signaling mediators, and to assess the acute effects of inhaled nitric oxide (NO) on pulmonary hemodynamics and gas exchange, at rest and during exercise. We evaluated seven patients with IPF (6 men/1 woman; 57 ± 11 yr; forced vital capacity, 60 ± 13% predicted; carbon monoxide diffusing capacity, 52 ± 10% predicted). Levels of endothelin, 6-keto-prostaglandin-F1α, thromboxane B2, and nitrates were measured at rest and during submaximal exercise. Pulmonary hemodynamics and gas exchange, including ventilation-perfusion relationships, were assessed breathing ambient air and 40 ppm NO, both at rest and during submaximal exercise. The concentration of thromboxane B2 increased during exercise ( P = 0.046), whereas levels of other mediators did not change. The change in 6-keto-prostaglandin-F1α correlated with that of mean pulmonary arterial pressure ( r = 0.94; P < 0.005). Inhaled NO reduced mean pulmonary arterial pressure at rest (−4.6 ± 2.1 mmHg) and during exercise (−11.7 ± 7.1 mmHg) ( P = 0.001 and P = 0.004, respectively), without altering arterial oxygenation or ventilation-perfusion distributions in any of the study conditions. Alveolar-to-capillary oxygen diffusion limitation, which accounted for the decrease of arterial Po2 during exercise, was not modified by NO administration. We conclude that, in IPF, some endothelium-derived signaling molecules may modulate the development of pulmonary hypertension during exercise, and that the administration of inhaled NO reduces pulmonary vascular resistance without disturbing gas exchange.

scholarly journals Mildly Elevated Pulmonary Arterial Pressure Is Associated With a High Risk of Progression to Pulmonary Hypertension and Increased Mortality: A Systematic Review and Meta‐Analysis

2021 ◽  
Author(s):  
Lin Xue ◽  
Yicheng Yang ◽  
Bo Sun ◽  
Bingyang Liu ◽  
Qixian Zeng ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Right Heart Catheterization ◽  
Heart Catheterization ◽  
Right Heart ◽  
Upper Limit ◽  
Increased Risk ◽  
Risk Of Progression ◽  
Pulmonary Arterial

Background Pulmonary hypertension (PH) is defined as a mean pulmonary arterial pressure (PAP) ≥25 mm Hg measured by right heart catheterization. However, the upper limit of a normal mean PAP is 20 mm Hg. There is a gap between the upper limit of normal and the threshold for diagnosing PH. Therefore, we aimed to investigate whether individuals with a mildly elevated PAP, defined as 20 mm Hg < mean PAP <25 mm Hg, are at an increased risk of progression to PH or mortality than those with a normal PAP. Methods and Results We reviewed studies evaluating the risk of progression to PH and/or mortality in individuals with a mildly elevated PAP versus those with a normal PAP. The mean PAP value of each participant was confirmed by right heart catheterization. We reviewed 1213 studies and 8 fulfilled our inclusion criteria. Our results indicated that individuals with a mildly elevated PAP were 1.81 to 2.45 times more likely to progress to PH than individuals with a normal PAP. There was a statistically significant difference in mortality between the mildly elevated PAP and normal PAP groups (hazard ratio, 2.48; 95% CI, 1.69–3.64). We also pooled survival probabilities in each arm to obtain a summary survival curve for each group, and the pooled survival rates in the mildly elevated PAP group were numerically lower than those in the normal PAP group. Conclusions Our study revealed that individuals with a mildly elevated PAP were at an increased risk of progression to PH and mortality than those with a normal PAP.

Pulmonary Hypertension May Be a Relevant Comorbidity in Patients with Myelodysplastic Syndromes

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 5039-5039 ◽  
Author(s):  
Xhylsime Kqiku ◽  
Gabor Kovacs ◽  
Sonja Reitter ◽  
Heinz Sill ◽  
Horst Olschewski
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Myelodysplastic Syndromes ◽  
Doppler Echocardiography ◽  
Pulmonary Arterial Pressure ◽  
Left Ventricular ◽  
Functional Class ◽  
Increased Risk ◽  
Pulmonary Arterial

Abstract Abstract 5039 Background: Pulmonary hypertension (PH) is characterized by elevated pulmonary arterial pressure and increased pulmonary vascular resistance, leading to right-sided heart failure and death. PH is defined as an increase in mean pulmonary arterial pressure (mPAP) ≥25 mmHg at rest. PAP values can be non-invasively estimated by Doppler echocardiography while right heart catheterization is needed for definite diagnosis. Hematologic disorders are associated with PH but it is unknown if myelodysplastic syndromes (MDS) bear an increased risk for PH. The objective of this study was to investigate the prevalence of PH in patients with MDS. Patients and Methods: From March 2009 to July 2011 consecutive MDS patients were recruited from the Hematology Division of the Medical University of Graz and enrolled in this PH screening program. All patients underwent Doppler echocardiography. PH was suspected if resting systolic pulmonary arterial pressure (SPAP) exceeded 40 mmHg. Additionally six minute walk distance (6MWD), pulmonary function test (PFT), laboratory tests including N-terminal pro brain natriuretic peptide (NT-proBNP), IPSS Score and WHO functional class were determined. Results: Fourty four MDS patients (female:male=18:26, age 70±12 years, disease onset 5±8 years, NYHA functional class I:II:III:IV=21:16:7:0, IPSS low/intermediate-I/intermediate- II/high/unknown=16:14:8:3:3; hemoglobin: 11±2 g/dl, white blood cell count 4±3 g/l; platelet count 159±125 g/l; regular transfusions n=19; WHO Classification: RCUD/RARS/RCMD/MDS del(5q)/RAEBI/RAEB II/MDSU=2:3:21:2:6:6:4 ) were included. Six patients had elevated SPAP (PH group, SPAP: 56±9mmHg) vs. 38 patients with normal values (SPAP 29±5mmHg). PH group were slightly older (79±9 vs. 69±11 years, p=0.53), had a decreased right ventricular function (TAPSE: 18±5mm vs. 22±4mm, p=0.05), a larger left atrium (46±5mm vs. 36±9mm measured in the parasternal long axis, p=0.005), a slightly decreased left ventricular systolic function (fractional shortening: 30±11% vs. 38±9 %, p=0.1) a significantly lower 6MWD (275±117m vs. 438±105m, p=0.01) and higher NT proBNP (4515±4732 pg/ml vs. 313±252 pg/ml, p=0.001) than patients with normal SPAP. In 4/6 PH group patients a relevant diastolic dysfunction of the left ventricle was suggested by echocardiography. Conclusion: According to our data, PH is present in about 15% of MDS patients and is associated with decreased physical capacity and heart failure. This suggests that PH may be considered as a relevant comorbidity in this cohort of patients. The reason of PAP increase may be multifactorial, postcapillary factors probably playing a relevant role. Disclosures: No relevant conflicts of interest to declare.

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